Does troncular vagotomy modify the proliferative gastric lesions induced in rats by duodenogastric reflux<A HREF="#back2"></A>?<A HREF="#back2"></A>

Abstract

Purpose: to investigate if combining VT to DGR through the pylorus can modulate the biological behavior of PL induced by DGR and to verify if TV alone can induce morphologic lesions in the gastric mucosa. Methods: 62 male Wistar rats were assigned to four groups: 1 -Control (CT) gastrotomy; 2 -Troncular Vagotomy (TV) plus gastrotomy; 3 -Duodenogastric reflux through the pylorus (R) and 4 -Troncular vagotomy plus DGR (RTV). The animals were killed at the 54 week of the experiment. DGR was obtained by anastomosing a proximal jejunal loop to the anterior gastric wall. TV was performed through isolation and division of the vagal trunks. Gastrotomy consisted of 1 cm incision at the anterior gastric wall. PL were analyzed gross and histologically in the antral mucosa, at the gastrojejunal stoma and at the squamous portion of the gastric mucosa. Results: Groups R and RTV developed exophytic lesions in the antral mucosa (R=90.9%; RTV=100%) and at the gastrojejunal stoma (R=54.54%; RTV=63.63%). Histologically they consisted of proliferative benign lesions, without cellular atypias, diagnosed as adenomatous hyperplasia. Both groups exposed to DGR presented squamous hyperplasia at the squamous portion of the gastric mucosa (R= 54.5%; RTV= 45.4%). TV, alone, did not induce gross or histological alterations in the gastric mucosa. TV did note change the morphologic pattern of the proliferative lesions induced by DGR. Conclusions: DGR induces the development of PL in the pyloric mucosa and at the gastrojejunal stoma. TV does not change the morphologic pattern of the proliferative lesions induced by DGR. TV alone is not able to induce morphologic lesions in the gastric mucosa. Key words: Vagotomy, Truncal. Duodenogastric Reflux. Hyperplasia. Rats. RESUMOObjetivo: investigar se a adição da VT ao RDG através do piloro, interfere no comportamento biológico das LP induzidas pelo RDG e observar se a VT isoladamente leva ao desenvolvimento de lesões morfológicas na mucosa gástrica. Métodos: Foram utilizados 62 ratos Wistar machos, distribuídos em quatro grupos experimentais: 1-Controle (CT) Gastrotomia; 2-Vagotomia Troncular + gastrotomia (VT); 3-Refluxo duodeno-gástrico (R) e 4-RDG através do piloro e VT (RTV). Os animais foram sacrificados na 54 a semana do experimento. O RDG foi obtido através de anastomose do jejuno proximal com a parede gástrica anterior. A vagotomia troncular foi realizada através da dissecção e divisão dos troncos vagais. A gastrotomia consistiu de secção e síntese de um cm na parede gástrica anterior. As LP foram analisadas macroscopicamente e histologicamente na mucosa gástrica, na anastomose gastrojejunal e no estômago escamoso. Resultados: Os grupos R e RVT desenvolveram lesões exofíticas na mucosa do antro gástrico (R=90,9% e RVT=100%) e na anastomose gastrojejunal (R=54,5% e RVT=63,6%) que se caracterizaram no exame histológico por lesões proliferativas epiteliais benignas, sem atipias celulares, diagnosticadas como hiperplasia adenomatosa. Na região do estômago escamoso, ambos os grupos exposto...

Correlation of precancerous lesion incidence with duodenogastric reflux and N-nitroso compound duration at reflux and antireflux stomach surgery: An experimental study

“…The specific finding in our study is the incidence of such a large percentage of cancer and dysplastic changes in the B2 group (conditionally refluxed) after 24 weeks of the experiment, since the time of DGR and MNNG action is relatively short, compared to other researchers, where the timelines of the experiments were 40, 90 and even 120 weeks [22][23][24][25][26] . These results suggest that the time of influence of DGR in the presence of MNNG is in direct correlation with the severity of precancerous lesions and that the minimum time of the occurrence of cancer is 20 weeks after the start of the experiment.…”

The role of duodenogastric reflux in formation of precarcinogenic gastric lesions: An experimental study

“…In experiments with animals, DGR induces mucosal corpus changes prior to carcinoma development or around the carcinomaaffected site. These changes include a loss of specific cells, hyperplasia of mucosal elements, adenocystic glandular proliferation, erosions and ulcer [17,18]. In addition, DGR enhances cell proliferation, extends cell cycle time and S-phase in corpus mucosa [19].…”

Omeprazole and adenocarcinoma in the stomach of rats submitted to duodenogastric reflux. Is there a protective effect?

“…The protocol for the histological analysis was prepared, including the following criteria 11 , 15 , 18 :…”

“…The gastric mucosa is particularly susceptible to the development of proliferative lesions when subjected to reflux of the duodenal contents, and some studies are directed to assess the possible relationship between primary duodenogastric reflux and the occurrence of neoplasia 9,10 . Furthermore, clinical and experimental studies have been carried out to investigate whether surgical techniques that promote duodenogastric reflux may be involved in the development of gastric cancer 11,12 . The intensity of glandular atrophy and intestinal metaplasia is directly related to the reflux of duodenal secretions to the gastric mucosa 13,14 .…”

“…The protocol for the histological analysis was prepared, including the following criteria 11,15,18 : Squamous Hyperplasia (SH) -Squamous epithelium thicker than normal twice or more, with hyperkeratosis.…”